Differential Diagnosis of Metabolic Acidosis

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Elevated anion gap acidoses

The elevation of the anion gap is created by inorganic (eg, phosphate, or sulfate), organic (eg, ketoacids or lactate), or exogenous (eg, salicylates) acids incompletely neutralized by bicarbonate. The most common etiologies of elevated anion gap acidoses can be remembered using the mnemonic MUDPILES: methanol, uremia, diabetic and alcoholic ketoacidosis, paraldehyde, isoniazid or iron, lactate, ethylene glycol, and salicylates (Box 1). A subsegment of these elevated anion gap acidoses are

Hyperchloremic or normal anion gap acidoses

The presence of a hyperchloremic or normal anion gap acidosis occurs by means of an excessive loss of HCO3 or an inability to excrete H+. HCO3 can be lost from the GI tract or from the kidneys, whereas, the inability to excrete H+ is a result of renal failure. More recent literature advocates calculation of a urinary anion gap (UAG) to aid in differentiating etiologies of an existing hyperchloremic acidosis. Although a negative UAG suggests GI HCO3 loss, a positive UAG indicates inability to

Summary

Although the presence and etiology of a metabolic acidosis in a tachypnic, dehydrated patient with a sweet odor on his or her breath and complaints of vomiting and polyuria is obvious, the physician is rarely so fortunate. More often, a metabolic acidosis must be confirmed by means of a simultaneous arterial blood gas and an electrolyte panel. Serum anion gap must be calculated to differentiate between an elevated gap and normal gap acidosis. The applicable mnemonic must be recalled, and each

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